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BACKGROUND: The diagnosis, severity assessment, and development of therapeutic strategies for asthma are crucial aspects of disease management. Since biomarkers are reliable tools in disease management, we aimed to identify and explore asthma-associated biomarkers and investigate their mechanisms. METHODS: Lipidomics was used to profile serum glycerophospholipids in asthmatic patients and controls. The absolute concentration of lysophosphatidylglycerol (LPG) 18:0 was quantified in various asthma subtypes. Mouse asthma models were used to confirm its potential as a biomarker and investigate its mechanisms in vivo. The effects of LPG 18:0 on CD4+ T cell differentiation, proliferation, and apoptosis were assessed in vitro by flow cytometry, while mitochondrial dysfunction was evaluated through mitochondrial membrane potential, reactive oxygen species, and ATP production measurements. The intracellular mechanism of LPG 18:0 in Tregs was investigated using small molecule inhibitors. RESULTS: The serum glycerophospholipid profile varied between asthmatic patients and control group, with LPG 18:0 levels being notably higher in asthmatic patients, correlating with asthma severity and control level. In vivo and in vitro studies revealed that LPG18:0 impaired naïve CD4+ T cell differentiation into Tregs and compromised their suppressive function. Further investigation demonstrated that LPG18:0 treatment reduced the FOXP3 protein level via SIRT1-mediated deacetylation during Treg differentiation. CONCLUSIONS: This study identifies that serum levels of LPG 18:0 are generally elevated in asthmatics and serve as a biomarker for asthma. LPG 18:0 impairs Treg function via the NAD+/SIRT1/FOXP3 pathway. Our research reveals the potential of LPG18:0 as a biomarker for asthma, elucidating its role in asthma diagnosis and treatment.
ABSTRACT
Severe fever with thrombocytopenia syndrome is an emerging viral hemorrhagic fever caused by a tick-borne bunyavirus, severe fever with thrombocytopenia syndrome virus (SFTSV), with a high case fatality. We previously found that SFTSV nucleoprotein (NP) induces macroautophagy/autophagy to facilitate virus replication. However, the role of NP in antagonizing host innate immunity remains unclear. Mitophagy, a selected form of autophagy, eliminates damaged mitochondria to maintain mitochondrial homeostasis. Here, we demonstrate that SFTSV NP triggers mitophagy to degrade MAVS (mitochondrial antiviral signaling protein), thereby blocking MAVS-mediated antiviral signaling to escape the host immune response. Mechanistically, SFTSV NP translocates to mitochondria by interacting with TUFM (Tu translation elongation factor, mitochondrial), and mediates mitochondrial sequestration into phagophores through interacting with LC3, thus inducing mitophagy. Notably, the N-terminal LC3-interacting region (LIR) motif of NP is essential for mitophagy induction. Collectively, our results demonstrated that SFTSV NP serves as a novel virulence factor, inducing TUFM-mediated mitophagy to degrade MAVS and evade the host immune response.
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PURPOSE: Postoperative surgical site infection is one of the most serious complications following spine surgery. Previous studies have reported Modic changes (MC) represent a subclinical infection. This study aims to investigate the relation between Modic changes and surgical site infection after posterior lumbar fusion surgery. METHODS: We retrospectively reviewed the records of 424 patients who received posterior lumbar fusion. Preoperative clinical and radiological parameters were recorded. Primary outcome was the rate of postoperative surgical site infection. Covariates included age, body mass index (BMI), sex, hypertension, diabetes mellitus, chronic heart failure, Pfirrmann classification, fused levels, and operation duration. The presence of Modic changes was used as an exposition variable, and adjusted for other risk factors in multivariate analyses. RESULTS: Of the 424 patients, 30 (7%) developed an acute surgical site infection. Infection had no relation to age, sex, BMI, and comorbidities. There were 212 (50%) patients with MC, and 23 (10.8%) had a surgical site infection, compared to 212 (50%) patients without MC in which there were 7 (3.3%) surgical site infections. MC was associated with surgical site infection in univariate analysis (odds ratio [OR] = 3.56, 95% confidence interval [CI]: 1.49-8.50, p = 0.004) and multivariate logistic regression analysis (OR = 3.05, 95% CI: 1.26-7.37, p = 0.013). There was statistically significant between specific type (p = 0.035) and grade of MCs (p = 0.0187) and SSI. CONCLUSIONS: MCs may be a potential risk factor for SSI following posterior lumbar spinal intervertebral fusion. Type I and grade C MCs showed a higher infection rate compared with other MC types and grades.
Subject(s)
Lumbar Vertebrae , Spinal Fusion , Surgical Wound Infection , Humans , Spinal Fusion/adverse effects , Male , Surgical Wound Infection/epidemiology , Surgical Wound Infection/etiology , Female , Middle Aged , Lumbar Vertebrae/surgery , Retrospective Studies , Aged , Risk Factors , AdultABSTRACT
Severe fever with thrombocytopenia syndrome virus (SFTSV) nonstructural protein (NSs) is an important viral virulence factor that sequesters multiple antiviral proteins into inclusion bodies to escape the antiviral innate immune response. However, the mechanism of the NSs restricting host innate immunity remains largely elusive. Here, we found that the NSs induced complete macroautophagy/autophagy by interacting with the CCD domain of BECN1, thereby promoting the formation of a BECN1-dependent autophagy initiation complex. Importantly, our data showed that the NSs sequestered antiviral proteins such as TBK1 into autophagic vesicles, and therefore promoted the degradation of TBK1 and other antiviral proteins. In addition, the 8A mutant of NSs reduced the induction of BECN1-dependent autophagy flux and degradation of antiviral immune proteins. In conclusion, our results indicated that SFTSV NSs sequesters antiviral proteins into autophagic vesicles for degradation and to escape antiviral immune responses.
ABSTRACT
Cyanide is a typical toxic reducing agent prevailing in wastewater with a well-defined chemical mechanism, whereas its exploitation as an electron donor by microorganisms is currently understudied. Given that conventional denitrification requires additional electron donors, the cyanide and nitrogen can be eliminated simultaneously if the reducing HCN/CN- and its complexes are used as inorganic electron donors. Hence, this paper proposes anaerobic cyanides oxidation for nitrite reduction, whereby the biological toxicity and activity of cyanides are modulated by bimetallics. Performance tests illustrated that low toxicity equivalents of iron-copper composite cyanides provided higher denitrification loads with the release of cyanide ions and electrons from the complex structure by the bimetal. Both isotopic labeling and Density Functional Theory (DFT) demonstrated that CN--N supplied electrons for nitrite reduction. The superposition of chemical processes reduces the biotoxicity and enhances the biological activity of cyanides in the CN-/Fe3+/Cu2+/NO2- coexistence system, including complex detoxification of CN- by Fe3+, CN- release by Cu2+ from [Fe(CN)6]3-, and NO release by nitrite substitution of -CN groups. Cyanide is the smallest structural unit of C/N-containing compounds and serves as a probe to extend the electron-donating principle of anaerobic cyanides oxidation to more electron-donor microbial utilization.
Subject(s)
Copper , Cyanides , Iron , Nitrites , Oxidation-Reduction , Cyanides/toxicity , Cyanides/chemistry , Nitrites/chemistry , Nitrites/toxicity , Copper/chemistry , Copper/toxicity , Anaerobiosis , Iron/chemistry , Water Pollutants, Chemical/toxicity , Water Pollutants, Chemical/chemistry , Wastewater/chemistry , Wastewater/toxicity , Denitrification/drug effectsABSTRACT
Herpesviruses are large double-stranded DNA viruses that cause infections in animals and humans with a characteristic of latent infectious within specific tissues. Bats are natural hosts of variety human-infecting viruses and recently have been described as hosts for herpesviruses in several countries around the world. In this study we collected 140 insectivorous bats in the neighboring urban areas of Wuhan City, Hubei Province in the central China between 2020 and 2021. Nested PCR targeting the dpol gene sequence indicated that a total of 22 individuals (15.7% of the sample) tested positive for herpesvirus with 4 strains belonging to the genus Betaherpesvirus and the remaining 18 strains classified as Gammahersvirus. Furthermore, the herpesvirus prevalence in Rhinolophus pusillus was higher at 26.3%, compared to 8.4% in Myotis davidii. The RP701 strain from R. pusillus was the predominant gammaherpesvirus strain detected in bats, accounting for 94.4% (17/18) of all strains. The variations in γ-herpesviruses genomic sequences was evident in phylogenetic tree, where RP701 strain was clustered together with ruminant γ-herpesviruses, while MD704 strain formed a distinct clade with a hedgehog γ-herpesvirus. Four betaherpesviruses exclusively identified from M. davidii, with nucleotide identities ranging from 79.7 to 82.6% compared to known betaherpesviruses. Our study provided evidence that M. davidii can sever as natural host for ß-herpesviruses, which extended the host species range. In conclusion, we found that bats from central China harbored novel ß-herpesviruses and γ-herpesviruses which were phylogenetically related to ruminant γ-herpesvirus and hedgehog γ-herpesvirus. Our study indicates that bats are natural hosts of ß- and γ-herpesviruses and further studies are needed to determine whether there is cross-species transmission of herpesviruses between bats and other animals, or humans.
Subject(s)
Betaherpesvirinae , Chiroptera , Gammaherpesvirinae , Herpesviridae Infections , Phylogeny , Animals , Chiroptera/virology , China/epidemiology , Gammaherpesvirinae/genetics , Gammaherpesvirinae/isolation & purification , Gammaherpesvirinae/classification , Betaherpesvirinae/genetics , Betaherpesvirinae/isolation & purification , Betaherpesvirinae/classification , Herpesviridae Infections/veterinary , Herpesviridae Infections/virology , Herpesviridae Infections/epidemiology , Genome, Viral , DNA, Viral/geneticsABSTRACT
BACKGROUND: In the beef industry, bull calves are usually castrated to improve flavor and meat quality; however, this can reduce their growth and slaughter performance. The gut microbiota is known to exert a significant influence on growth and slaughter performance. However, there is a paucity of research investigating the impact of castration on gut microbiota composition and its subsequent effects on slaughter performance and meat flavor. RESULT: The objective of this study was to examine the processes via which castration hinders slaughter productivity and enhances meat quality. Bull and castrated calves were maintained under the same management conditions, and at slaughter, meat quality was assessed, and ileum and epithelial tissue samples were obtained. The research employed metagenomic sequencing and non-targeted metabolomics techniques to investigate the makeup of the microbiota and identify differential metabolites. The findings of this study revealed the Carcass weight and eye muscle area /carcass weight in the bull group were significantly higher than those in the steer group. There were no significant differences in the length, width, and crypt depth of the ileum villi between the two groups. A total of 53 flavor compounds were identified in the two groups of beef, of which 16 were significantly higher in the steer group than in the bull group, and 5 were significantly higher in the bull group than in the steer group. In addition, bacteria, Eukaryota, and virus species were significantly separated between the two groups. The lipid metabolism pathways of α-linolenic acid, linoleic acid, and unsaturated fatty acids were significantly enriched in the Steers group. Compared with the steer group, the organic system pathway is significantly enriched in the bull group. The study also found that five metabolites (LPC (0:0/20:3), LPC (20:3/0:0), LPE (0:0/22:5), LPE (22:5/0:0), D-Mannosamine), and three species (s_Cloning_vector_Hsp70_LexA-HP1, s_Bacteroides_Coprophilus_CAG: 333, and s_Clostridium_nexile-CAG: 348) interfere with each other and collectively have a positive impact on the flavor compounds of beef. CONCLUSIONS: These findings provide a basic understanding that under the same management conditions, castration does indeed reduce the slaughter performance of bulls and improve the flavor of beef. Microorganisms and metabolites contribute to these changes through interactions.
Subject(s)
Gastrointestinal Microbiome , Ileum , Red Meat , Animals , Cattle , Male , Red Meat/microbiology , Ileum/microbiology , Ileum/metabolism , MetabolomicsABSTRACT
Fractures are frequent and severe musculoskeletal injuries. This study aimed to investigate the function of tenascin-C (TNC) in regulating chondrogenic during fracture healing and elucidate the underlying molecular mechanisms. A well-established femur fracture model in male C57BL/6J mice was used to transect the middle diaphysis of the femur. To identify the essential role of TNC, shTNC lentiviruses or TNC protein were administered in the animal model. Micro-CT analysis, histologic analysis, immunostaining assays, and gene expression analysis were employed to investigate the effect of TNC during fracture healing. An in vitro mesenchymal stem cell culture system was developed to investigate the role and molecular mechanism of TNC in regulating chondrogenesis. TNC expression was induced at the inflammatory phase and peaked at the cartilaginous callus phase during fracture healing. Knockdown of TNC expression in callus results in decreased callus formation and impaired fracture healing. Conversely, administration of exogenous TNC promoted chondrogenic differentiation, cartilage template formation and ultimately improved fracture healing. Both the Hedgehog and Hippo signaling pathways were found to be involved in the pro-chondrogenic function of TNC. Our observations demonstrate that TNC is a crucial factor responsible for endochondral ossification in fracture healing and provide a potential therapeutic strategy for promoting fracture healing.
Subject(s)
Femoral Fractures , Fracture Healing , Osteogenesis , Tenascin , Animals , Male , Mice , Bony Callus/pathology , Femoral Fractures/pathology , Hedgehogs , Hippo Signaling Pathway , Mice, Inbred C57BL , Tenascin/genetics , Tenascin/metabolismABSTRACT
Background: An experimental study was performed to improve the anterior approach model of intervertebral disc degeneration (IVDD). Objective: The aims of this study were to investigate the anterior approach model of IVDD for the cause of death, phenotypes, and underlying mechanisms of low back pain in mice. Method: In this study, we conducted an anterior puncture procedure on a cohort of 300 C57BL/6J mice that were 8 weeks old. Our investigation focused on exploring the causes of death in the study population (n = 300) and assessing the time-course changes in various parameters, including radiographical, histological, immunofluorescence, and immunohistochemistry analyses (n = 10). Additionally, we conducted behavioral assessments on a subset of the animals (n = 30). Results: Transverse vertebral artery rupture is a major factor in surgical death. Radiographical analyses showed that the hydration of the nucleus pulposus began to decrease at 2 weeks after puncture and obviously disappeared over 4 weeks. 3D-CT showed that disc height was significantly decreased at 4 weeks. Osteophyte at the anterior vertebral rims was observed at 2 weeks after the puncture. As the time course increased, histological analyses showed progressive disruption of the destruction of the extracellular matrix and increased secretion of inflammatory cytokines and apoptosis. Behavioral signs of low back pain were increased between the puncture and sham groups at 4 weeks. Conclusion: The improvement of anterior intervertebral disc approach model in mice will be useful to investigate underlying mechanisms and potential therapeutic strategies for behavior and phenotypes. Furthermore, the application of vibrational pre-treatment can be used to increase the sensitivity of axial back pain in the model, thereby providing researchers with a reliable method for measuring this critical phenotype.
ABSTRACT
Intervertebral disc degeneration is a natural process during aging and a leading cause of lower back pain. Here, we generate a comprehensive atlas of nucleus pulposus cells using single-cell RNA-seq analysis of human nucleus pulposus tissues (three males and four females, age 41.14 ± 18.01 years). We identify fibrotic late-stage nucleus pulposus cells characterized by upregulation of serglycin expression which facilitate the local inflammatory response by promoting the infiltration of inflammatory cytokines and macrophages. Finally, we discover that daphnetin, a potential serglycin ligand, substantially mitigates the local inflammatory response by downregulating serglycin expression in an in vivo mouse model, thus alleviating intervertebral disc degeneration. Taken together, we identify late-stage nucleus pulposus cells and confirm the potential mechanism by which serglycin regulates intervertebral disc degeneration. Our findings indicate that serglycin is a latent biomarker of intervertebral disc degeneration and may contribute to development of diagnostic and therapeutic strategies.
Subject(s)
Intervertebral Disc Degeneration , Intervertebral Disc , Nucleus Pulposus , Male , Female , Humans , Animals , Mice , Young Adult , Adult , Middle Aged , Intervertebral Disc Degeneration/metabolism , Nucleus Pulposus/metabolism , Proteoglycans , Biomarkers , Intervertebral Disc/metabolismABSTRACT
This study investigated the molecular mechanism by which acetylshikonin inhibits SOX4 expression via the PI3K/Akt pathway to delay intervertebral disc degeneration (IVDD) and low back pain (LBP). Bulk RNA-seq, RT-qPCR, Western blot analysis, immunohistochemical staining, small interfering RNA (siSOX4), lentivirus (lentiv-SOX4hi ), and imaging techniques were used to assess SOX4 expression and validate its upstream regulatory pathway. Acetylshikonin and siSOX4 were injected into the IVD to measure IVDD. SOX4 expression significantly increased in degenerated IVD tissues. TNF-α increased SOX4 expression and apoptosis-related proteins in nucleus pulposus cells (NPCs). siSOX4 reduced TNF-α-induced NPCs apoptosis, while Lentiv-SOX4hi increased it. The PI3K/Akt pathway was significantly correlated with SOX4, and acetylshikonin upregulated PI3K/Akt pathway while inhibiting SOX4 expression. In the anterior puncture IVDD mouse model, SOX4 expression was upregulated, and acetylshikonin and siSOX4 delayed IVDD-induced LBP. Acetylshikonin delays IVDD-induced LBP by inhibiting SOX4 expression through the PI3K/Akt pathway. These findings offer potential therapeutic targets for future treatments.
Subject(s)
Intervertebral Disc Degeneration , Intervertebral Disc , Low Back Pain , Nucleus Pulposus , Animals , Mice , Apoptosis , Intervertebral Disc/metabolism , Intervertebral Disc Degeneration/drug therapy , Low Back Pain/drug therapy , Nucleus Pulposus/metabolism , Phosphatidylinositol 3-Kinases , Proto-Oncogene Proteins c-akt , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Plasmon-mediated electrochemistry is an emerging area of interest in which the electrochemical reactions are enhanced by employing metal nanostructures possessing localized surface plasmon resonance (LSPR). However, the reaction efficacy is still far below its theoretical limit due to the ultrafast relaxation of LSPR-generated hot carriers. Herein, we introduce p-hydroxythiophenol (PHTP) as a molecular cocatalyst to significantly improve the reaction efficacy in plasmon-mediated electrochemical oxidation of p-aminothiophenol (PATP) on gold nanoparticles. Using electrochemical techniques, in situ Raman spectroscopy, and theoretical calculations, we elucidate that the presence of PHTP improves the hot hole-mediated electrochemical oxidation of PATP by 2-fold through the trapping of plasmon-mediated hot electrons. In addition, the selectivity of PATP oxidation could also be modulated by the introduction of PHTP cocatalyst. This tactic of employing molecular cocatalyst can be drawn out to endorse various plasmonic electrochemical reactions because of its simple protocol, high efficiency, and high selectivity.
ABSTRACT
N-acetylglucosamine (GlcNAc) is significant functional monosaccharides with diverse applications in medicine, food, and cosmetics. In this study, the GlcNAc synthesis pathway was constructed in Corynebacterium glutamicum and its reverse byproduct pathways were blocked. Simultaneously the driving force of GlcNAc synthesis was enhanced by screening key gene sources and inhibiting the GlcNAc consumption pathway. To maximize carbon flux, some competitive pathways (Pentose phosphate pathway, Glycolysis pathway and Mannose pathway) were weakened and the titer of GlcNAc reached 23.30 g/L in shake flasks. Through transcriptome analysis, it was found that dissolved oxygen was an important limiting factor, which was optimized in a 5 L bioreactor. Employing optimal fermentation conditions and feeding strategy, the titer of GlcNAc reached 138.9 g/L, with the yeild of 0.44 g/g glucose. This study significantly increased the yield and titer of GlcNAc, which lay a solid foundation for the industrial production of GlcNAc in C. glutamicum.
Subject(s)
Corynebacterium glutamicum , Corynebacterium glutamicum/genetics , Corynebacterium glutamicum/metabolism , Acetylglucosamine/genetics , Acetylglucosamine/metabolism , Metabolic Engineering , Bioreactors , FermentationABSTRACT
BACKGROUND: The order Rickettsiales contains a group of vector-borne gram-negative obligate intracellular bacteria, which often cause human emerging infectious diseases and economic losses for dairy and meat industries. The purpose of this study is to investigate the distribution of the pathogens including Rickettsia spp., Anaplasma spp., and Ehrlichia spp. in the order Rickettsiales in ticks from Yueyang, a prefecture-level city of Hunan Province in Sothern China, and assess the potentiality of transovarial transmission of these rickettsial organisms. METHODS: Ticks were collected from cattle in a farm in Yueyang City and the tick DNA was used as template to amplify the htrA, rrs, gltA, ompA and ompB genes of Rickettsia as well as rrs and groEL genes of Anaplasma and Ehrlichia. RESULTS: All ticks (465) collected were the cattle tick, Rhipicephalus microplus. PCR showed the minimum infection rate (MIR) was 1.5% (7/465) for Candidatus Rickettsia xinyangensis, 1.9% (9/465) for C. Anaplasma boleense, 1.3% (6/465) for Anaplasma platys, 0.6% (3/465) for A. marginale, and 1.17% (2/465) for each of A. bovis, Ehrlichia minasensis, and a non-classified Ehrlichia sp. A human pathogen, C. Rickettsia xinyangensis and A. platys were detected in 100% (3/3) and 33.3% (2/6) laboratory-hatched larval pools from infected females respectively. CONCLUSION: Our study revealed a diversity of pathogenic rickettsial species in R. microplus ticks from Hunan Province suggesting a threat to people and animals in China. This study also provided the first molecular evidence for the potential transovarial transmission of C. Rickettsia xinyangensis and A. platys in R. microplus, indicating that R. microplus may act as the host of these two pathogens.
Subject(s)
Coleoptera , Rhipicephalus , Rickettsia , Animals , Female , Humans , Rickettsia/genetics , Larva , Ehrlichia/genetics , Rickettsiales , Anaplasma/geneticsABSTRACT
This study investigated the effects of NO2- on synergetic interactions between Anammox bacteria (AnAOB) and sulfur-oxidizing bacteria (SOB) in an autotrophic denitrification-Anammox system. The presence of NO2- (0-75 mg-N/L) was shown to significantly enhance NH4+ and NO3- conversion rates, achieving intensified synergy between AnAOB and SOB. However, once NO2- exceed a threshold concentration (100 mg-N/L), both NH4+ and NO3- conversion rates decreased with increased NO2- consumption via autotrophic denitrification. The cooperation between AnAOB and SOB was decoupled due to the NO2- inhibition. Improved system reliability and nitrogen removal performance was achieved in a long-term reactor operation with NO2- in the influent; reverse transcription-quantitative polymerase chain reaction analysis showed elevated hydrazine synthase gene transcription levels (5.00-fold), comparing to these in the reactor without NO2-. This study elucidated the mechanism of NO2- induced synergetic interactions between AnAOB and SOB, providing theoretical guidance for engineering applications of Anammox-based coupled systems.
Subject(s)
Denitrification , Nitrites , Nitrogen/analysis , Anaerobic Ammonia Oxidation , Nitrogen Dioxide/analysis , Reproducibility of Results , Bioreactors/microbiology , Bacteria , Oxidation-Reduction , Sulfur , Sewage/microbiologyABSTRACT
Strain sensors have been attracting tremendous attention for the promising application of wearable devices in recent years. However, the trade-off between high resolution, high sensitivity, and broad detection range is a great challenge for the application of strain sensors. Herein, a novel design of hierarchical synergistic structure (HSS) of Au micro cracks and carbon black (CB) nanoparticles is reported to overcome this challenge. The strain sensor based on the designed HSS exhibit high sensitivity (GF > 2400), high strain resolution (0.2%) even under large loading strain, broad detection range (>40%), outstanding stability (>12000 cycles), and fast response speed simultaneously. Further, the experiments and simulation results demonstrate that the carbon black layer greatly changed the morphology of Au micro-cracks, forming a hierarchical structure of micro-scale Au cracks and nano-scale carbon black particles, thus enabling synergistic effect and the double conductive network of Au micro-cracks and CB nanoparticles. Based on the excellent performance, the sensor is successfully applied to monitoring tiny signals of the carotid pulse during body movement, which illustrates the great potential in the application of health monitoring, human-machine interface, human motion detection, and electronic skin.
ABSTRACT
PURPOSE: In this study, we intended to investigate the association between immediate postoperative hypoalbuminemia and surgical site infection (SSI), and determine a threshold value for postoperative hypoalbuminemia that can assist in risk stratification in patients after posterior lumbar fusion surgery. METHODS: From January 2017 to December 2021, 466 consecutive patients who underwent posterior lumbar fusion surgery were selected to analyze the relationship between immediate postoperative hypoalbuminemia and SSI. Multivariate logistic regression analysis was performed to identify the independent risk factors of SSI and postoperative hypoalbuminemia. Receiver Operating Characteristic (ROC) analysis was used to determine the optimal value for postoperative hypoalbuminemia, and subsequent grouping was based on the identified threshold. RESULTS: Of the total 466 patients, 25 patients (5.4%) developed SSI after surgery, and lower postoperative albumin (OR: 0.716, 95% CI: 0.611-0.840, p < 0.001) was independently associated with SSI. ROC analysis showed that the cutoff value of postoperative hypoalbuminemia was 32 g/L with a sensitivity of 0.760, specificity of 0.844, and a Youden index of 0.604. Postoperative SSI was more common in patients with postoperative hypoalbuminemia than in those without (21.6% vs. 1.6%, p < 0.001). Age, gender and operative duration were found to be independent predictors of postoperative hypoalbuminemia. CONCLUSIONS: This study showed that immediate postoperative hypoalbuminemia was an independent risk factor for the development of SSI in patients who underwent posterior lumbar fusion. Even in patients with a normal preoperative serum albumin level, there was an increased risk of SSI when the postoperative albumin within 24 h was < 32 g/L.
Subject(s)
Hypoalbuminemia , Surgical Wound Infection , Humans , Surgical Wound Infection/epidemiology , Surgical Wound Infection/etiology , Hypoalbuminemia/epidemiology , Risk Factors , Albumins , Retrospective StudiesABSTRACT
Hydraulic retention time (HRT), as an important parameter in the wastewater treatment process, has a great impact on water quality and energy consumption. With the rapid advances in computer technology and deepened understanding of in microbial metabolism, a series of activated sludge models (ASMs) have been developed and applied in wastewater treatment. However, ASMs simulation based on the nexus of HRT, water treatment process, water quality and energy consumption has yet to be verified. In this study, HRT was creatively linked to water treatment process variation. And a novel combined process model (CPM) was developed based on the operational data and treatment performance data from 4 full-scale coking wastewater treatment processes. In the CPM, an array of biological treatment processes were represented by setting the HRT in respective treatment units of the anaerobic-oxic-hydrolytic & denitrification-oxic (A/O/H/O) process. The relationships between HRT, effluent quality and energy consumption were systematically analyzed. Results showed that: (i) for A/O/H/O process, the HRT of first oxic (O1) reactor has a key effect on the effluent water quality and energy consumption, while the impact of the anaerobic (A) reactor HRT was limited; (ii) the O/H/O process has a clear advantage in treating coking wastewater due to the carbon removal and detoxification function of O1 reactor; (iii) the lowest energy consumption (with the total system HRT below 210 h) to meet the biological effluent quality requirements (COD = 200 mg/L, TN = 50 mg/L) is 4.429 kWh/m3. Since the CPM could effectively work out the optimal process configuration and break the boundaries between HRT and process variation, it has enormous potential to be extended to the design of other wastewater treatment processes.
Subject(s)
Coke , Water Purification , Waste Disposal, Fluid/methods , Bioreactors , Wastewater , Sewage , AnaerobiosisABSTRACT
BACKGROUND: Many countries have already banned the use of antibiotics in animal husbandry, making it extremely difficult to maintain animal health in livestock breeding. In the livestock industry, there is an urgent need to develop alternatives to antibiotics which will not lead to drug resistance on prolonged use. In this study, eighteen castrated bulls were randomly divided into two groups. The control group (CK) was fed the basal diet, while the antimicrobial peptide group (AP) was fed the basal diet supplemented with 8 g of antimicrobial peptides in the basal diet for the experimental period of 270 d. They were then slaughtered to measure production performance, and the ruminal contents were isolated for metagenomic and metabolome sequencing analysis. RESULT: The results showed that antimicrobial peptides could improve the daily weight, carcass weight, and net meat weight of the experimental animals. Additionally, the rumen papillae diameter and the micropapillary density in the AP were significantly greater than those in the CK. Furthermore, the determination of digestive enzymes and fermentation parameters showed that the contents of protease, xylanase, and ß-glucoside in the AP were greater than those in the CK. However, lipase content in the CK was greater than that in the AP. Moreover, the content of acetate, propionate, butyrate, and valerate was found to be greater in AP than those in CK. The metagenomic analysis annotated 1993 differential microorganisms at the species level. The KEGG enrichment of these microorganisms revealed that the enrichment of drug resistance-related pathways was dramatically decreased in the AP, whereas the enrichment of immune-related pathways was significantly increased. There was also a significant reduction in the types of viruses in the AP. 187 probiotics with significant differences were found, 135 of which were higher in AP than in CK. It was also found that the antimicrobial mechanism of the antimicrobial peptides was quite specific. Seven low-abundance microorganisms (Acinetobacter_sp._Ac_1271, Aequorivita soesokkakensis, Bacillus lacisalsi, Haloferax larsenii, Lysinibacillus_sp._3DF0063, Parabacteroides_sp._2_1_7, Streptomyces_sp._So13.3) were found to regulate growth performance of the bull negatively. Metabolome analysis identified 45 differentially differential metabolites that significantly different between the CK and the AP groups. Seven upregulated metabolites (4-pyridoxic acid, Ala-Phe, 3-ureidopropionate, hippuric acid, terephthalic acid, L-alanine, uridine 5-monophosphate) improve the growth performance of the experimental animals. To detect the interactions between the rumen microbiome and metabolism, we associated the rumen microbiome with the metabolome and found that negative regulation between the above 7 microorganisms and 7 metabolites. CONCLUSIONS: This study shows that antimicrobial peptides can improve the growth performance of animals while resisting viruses and harmful bacteria and are expected to become healthy alternatives to antibiotics. We demonstrated a new antimicrobial peptides pharmacological model. We demonstrated low-abundance microorganisms may play a role by regulating the content of metabolites.